Pulmonary thromboembolism

Pulmonary thromboembolismPulmonary thromboembolism is responsible for up to 50,000 deaths each year. It is the third cause of death among hospitalized patients, yet only 30–40% of those with pulmonary thromboembolism have suspected deep venous thrombosis. Efforts directed at reduction in the mortality rate of pulmonary thromboembolism demand an aggressive approach to diagnosis of this problem in patients identified to be at high risk.

Pulmonary thromboembolisms arise from a number of sources. Air embolism can occur during the placement or removal of central venous catheters. Amniotic fluid emboli may occur during active labor. Fat emboli from long bone fractures cause a syndrome characterized by respiratory insufficiency, coagulopathy, encephalopathy, and an upper body petechial rash. Other less common causes of pulmonary emboli include septic emboli, tumor emboli from atrial myxoma or inferior vena cava extension of renal cell carcinoma, and parasitic emboli. However, DVT remains the most common source of pulmonary thromboemboli. Up to 60% of patients with untreated proximal lower extremity DVT may develop pulmonary thromboembolism.

Fewer than 10% of pulmonary thromboemboli will produce pulmonary infarction. Obstruction of large pulmonary arteries results in increases in pulmonary artery pressure and acute right ventricular failure, but many of the clinical manifestations of pulmonary thromboembolism result from release of vasoactive amines that cause severe pulmonary vasoconstriction. Vasoconstriction leads to increased physiologic dead space and systemic hypoxia from a right-to-left shunt. Reflex bronchial vasoconstriction is also common.

Symptoms and Signs of Pulmonary thromboembolism

Dyspnea and chest pain are present in up to 75% of patients. However, these symptoms are nonspecific, especially in patients who may have underlying cardiopulmonary disease. Tachycardia, tachypnea, and altered mental status are highly suggestive findings in an at-risk population. The classic triad of dyspnea, chest pain, and hemoptysis is present in only 15% of patients. Pleural friction rub and the S1Q3T3 morphology on electrocardiography are even less common findings.

Imaging and Other Diagnostic Studies

Chest x-ray is most often normal but may show a pleural cap. Electrocardiography may reveal new-onset atrial fibrillation or ischemic changes, but in most cases only acute sinus tachycardia and nonspecific ST and T wave changes are identified. Arterial blood gas determination reveals hypoxia and often a respiratory alkalosis or increased arterial-alveolar oxygen gradient. Plasma D-dimer levels are elevated in the presence of both pulmonary thromboembolism and acute DVT, but this test lacks sufficient specificity to be of primary diagnostic value.

Until recently, the most common studies used to diagnose pulmonary embolism were ventilation-perfusion (VQ) scan and pulmonary angiogram. Ventilation-perfusion scans have sensitivity and specificity that approach 90% if results of the scan correlate with clinical risk factor assessment. For example, treatment can be started in a patient with a high-probability scan and a highly suggestive examination. Unfortunately, two-thirds of studies are inconclusive. Pulmonary angiography remains the most reliable test for diagnosis, but it is invasive, time-consuming, and expensive.

Two newer modalities have improved the accuracy and safety of the diagnosis. Spiral CT scan has virtually replaced VQ scan in the diagnosis. Accuracy supersedes that of VQ scan and does not require clinical correlation. Magnetic resonance angiography has also demonstrated excellent sensitivity and specificity and is now being used in many institutions.

Treatment of Pulmonary thromboembolism

Anticoagulation

Heparin or LMWH anticoagulation is started as soon as the diagnosis is made after initial stabilization with ventilatory support and vasopressor medications. Thrombolysis is considered for large clot burden, severe respiratory compromise, or hemodynamic instability. When compared with heparin alone, thrombolytic therapy speeds the resolution of pulmonary emboli. The disadvantages of lytic therapy include its greater cost and higher risk of significant bleeding complications.

Inferior Vena Cava Interruption

It considered in patients who have extension of venous thrombus on adequate heparin therapy, patients in whom heparin anticoagulation is contraindicated. More recently, temporary or permanent inferior vena cava filters have been placed prophylactically in patients such as those with unresectable cancer or major trauma.

Historically, inferior vena cava interruption was performed as an open surgical procedure, involving ligation or plication of the infrarenal vena cava or placement of a serrated clip to “strain” blood returning to the right atrium. The Greenfield filter developed in 1973 was initially deployed by venous cutdown. Multiple devices are now available for fluoroscopically guided percutaneous placement through a 12F sheath introduced into the common femoral vein or, in cases of femoral thrombus, into the internal jugular vein. A duplicated inferior vena cava must be excluded by venography at the time of filter placement because lower extremity DVT might still serve as a source of emboli. Newer devices being developed today include those used for only a temporary period of time (retrievable filter). Additionally, devices are being deployed under ultrasound guidance.

Surgical Treatment

Hemodynamically unstable patients in whom thrombolysis has failed or cannot be instituted require percutaneous or open surgical extraction of the thrombus. Open surgical pulmonary embolectomy is reserved for patients who develop intractable hypotension, those who fail transcatheter pulmonary embolectomy, and those who have tumor or foreign body emboli. Catheter techniques involve mechanical thrombolysis or removal of intact pulmonary emboli using a suction cup embolectomy device.

Prognosis

Pulmonary embolism is the most frequent causes of preventable hospital death. Prevention by use of DVT prophylaxis and early diagnosis by selective testing of high-risk patients are essential steps to reducing the morbidity.

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